This retrospective study aimed to determine the value of pulmonary circulation in the assessment of the severity and tendency of severe and critical patients with COVID-19 pneumonia through chest CT images. Our study comprehensively described the major differences in pulmonary circulation on chest CT images between deceased patients and recovered patients with COVID-19. The severe phases and the improved phases of COVID-19 patients in the recovered group were also evaluated and compared. We found that evaluation in the diameters of pulmonary veins on chest CT images might be a useful tool for determining the severity and tendency of COVID-19. Furthermore, the dilation of PV was a predictor of poor clinical outcomes.
COVID-19 has caused far more infections and deaths than severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) due to its high infectivity, which have mortality rates of 9.6%[14] and 34.4%[15], respectively. Because no specialized drugs have been found to treat severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, the main treatment is timely symptomatic and supportive treatment [ 16 ]. Among patients with COVID-19, especially those who are severely and critically ill, SARS-CoV-2 primarily affects the lungs, it also affects multiple organs, such as the cardiovascular system [17]. However, to our knowledge, no study has been performed to evaluate pulmonary circulation on chest CT in COVID-19 pneumonia patients.
In our study, the diameters of pulmonary vein of the deceased patients were larger than recovered patients in the severe phase (p < 0.001), and compared with the initial CT, PVs were more dilated on the last CT before death in the deceased patients (all p < 0.05), which may indicate that the dilation of pulmonary vein in severe and critical patients with COVID-19 are at higher risk of death. Furthermore, construction of a ROC curve yielded an optimal cut-off value of the PV diameters for prediction of survival. We proposed that the dilation of PV was a predictor of poor clinical outcomes. The dilation of PV is seen in pulmonary congestion caused by increased pulmonary venous return and left heart insufficiency [18,19]. Pulmonary inflammation leads to congestion of the lung tissue, which has been reported in the early studies. Severe and critically patients have severe pulmonary infections, manifested by abnormal laboratory and radiographic findings, such as higher levels of WBC and h-CRP; more ground-glass opacities, consolidation and higher total CT stores. Therefore, obvious congestion might increase PV regurgitation, leading to the enlargement of PV. In recovered patients, the reduction of PV diameter accompanied by lower total CT score in the improved phase compared with in the severe phase, indicates the reduced of pulmonary circulation reflux and the absorption and improvement of pulmonary inflammation. In addition, the main target organ of the COVID-19 infection is the lung, and some recent studies have reported it could also cause myocardial damage [17,20]. Mechanistically, SARS-CoV-2, binds to the transmembrane angiotensin-converting enzyme 2 (ACE2), and then enters type 2 pneumocytes, macrophages, pericytes and cardiomyocytes [17]. High expression of ACE2 in pericytes could lead to development of microvascular dysfunction. ACE2 expression is up-regulated in failing human hearts, suggesting a plausible explanation for a higher infectivity of virus and a higher mortality in patients with heart failure. The significant increase of myocardial enzyme spectrum indicates that the myocardium is involved [5]. In our study, compared with the recovered patients, the deceased patients showed the significant increase of high-sensitivity troponin, lactic dehydrogenase and NT-proBNP, which was consistent with relevant reports and suggested myocardial injury and cardiac dysfunction [21]. Mechanisms underlying myocardial injury remain unclear. It is worthy of attention whether they reflect systemic or local process and ischaemic or inflammatory process. Also, since ACE2 (a homologue of ACE) is expressed in cardiomyocytes, direct cardiomyocyte infection by SARS-CoV-2 may be a possibility [17, 22 ]. Pulmonary congestion indirectly indicated left heart insufficiency, which is usually manifested as blurred hilar shadows and dilated PVs on CT images. CT examination clearly showed the hilar structure, so it has a unique advantage in determining whether the lesion involves the hilum. In our study, 36 cases (69%) of 52 deceased patients and 20 cases (42.55%) of 47 recovered patients shown hilar involvement on chest CT images(p=0.009). Some attempts to treat COVID-19 cardiac injury have done, the detection of pulmonary circulation, expecially pulmonary vein, might help identify a subset of patients at greater risk of COVID-19 complications and successful therapies. Therefore, the changes of PVs might indirectly reflect the activity of pulmonary inflammation and cardiac insufficiency. This new radiological evidence provided an innovative new method compared with previous investigations in the assessment of the severity of severe and critical patients with COVID-19.
The representative chest CT findings of patients with COVID-19 were peripheral and/or subpleural ground-glass opacities or consolidation for common patients [1]. Furthermore, in severe and critical COVID-19 pneumonia patients, more and more ground-glass attenuation and airspace consolidation as well as involvement of multiple lung lobes and high CT scores were common chest CT finding [23], which was similar in our study. Traditionally, more and more larger lesions on CT images indicates that the lung inflammation was more serious. However, we posed a hypothetical question which pulmonary manifestations of severe and critical COVID-19 pneumonia might be related to myocardial injury and cardiac insufficiency, expecially accompanied by dilated PVs.
This study has the following limitations: Firstly, it was a retrospective study. Secondly, there was a small sample size of COVID-19, thus some conclusions are preliminary. More powerful studies with pooled data from multiple centers is needed in our subsequent studies. Thirdly, no lung biopsy or autopsy was performed to reflect the histopathological changes.
In conclusion, the retrospective study suggests that chest CT should be considered as a quick and effective method to assess the changes in pulmonary circulation and the progression of COVID-19 pneumonia. Evaluation of changes in pulmonary circulation by chest CT images might be considered as a useful tool for determining the severity and tendency of COVID-19. The changes of PVs might indirectly reflect the activity of pulmonary inflammation and cardiac insufficiency. Pulmonary manifestations of severe and critical COVID-19 pneumonia might be related to myocardial injury and cardiac insufficiency, expecially accompanied by dilated PVs. In this way, the evolution of the patient's condition could be detected in time, and targeted treatment can be adopted, so as to improve the prognosis of patients and reduce the risk of death of severe patients, especially critical patients.